Prenatal Maternal Occupation and Child Epigenetic Age Acceleration in an Agricultural Region

Key Points Question Is prenatal maternal occupation associated with child epigenetic aging in a farmworker population? Findings In this cohort study of 290 mother-child pairs, children whose mothers engaged in agricultural fieldwork during pregnancy had greater epigenetic age acceleration as measured by several DNA methylation–based biomarkers compared with those whose mothers did not work during pregnancy. These associations were independent of sociodemographic characteristics and prenatal pesticide exposure. Meaning These findings suggest that children of agricultural fieldworkers, a vastly understudied population, may experience increased rates of biological aging early in life and greater risk of age-related diseases later in life due to prenatal stressors.


Intrinsic Epigenetic Age Acceleration
Estimated proportions of blood CD8 T cells, CD4 T cells, natural killer cells, B cells, monocytes, and granulocytes were generated by the Clock Foundation calculator 9 using the Houseman algorithm. 10The calculator also estimated intrinsic epigenetic age acceleration (IEAA), a residual value calculated by regressing Horvath epigenetic age on chronological age and adjusting for the estimated blood cell counts which are known to change with age.Regression coefficients in years and 95% CIs derived from linear mixed effects models with additional statistical interaction term between child age and prenatal maternal occupation.
Adjusted for sociodemographic covariates (maternal age at delivery, pre-pregnancy BMI, baseline maternal education, baseline maternal marital status, parity, poverty status during pregnancy, smoking and alcohol consumption during pregnancy, and child sex) and prenatal OP pesticide exposure (log10transformed mean prenatal urinary DAP concentrations and log2-transformed kilograms of OP pesticides used within 1 kilometer of maternal residence during pregnancy).Regression coefficients in years and 95% CIs derived from linear mixed effects models adjusted for sociodemographic covariates (maternal age at delivery, pre-pregnancy BMI, baseline maternal education, baseline maternal marital status, parity, poverty status during pregnancy, smoking and alcohol consumption during pregnancy, and child sex) and prenatal OP pesticide exposure (log10-transformed mean prenatal urinary DAP concentrations and log2-transformed kilograms of OP pesticides used within 1 kilometer of maternal residence during pregnancy). Outcomes

eFigure 1 .
Performance of six epigenetic clocks in CHAMACOS children (ages 7-14 years, N=290) Pearson correlation coefficient r and median absolute error (MAE) between child chronological age based on birth date and epigenetic age (EA) estimated by the (A) Horvath Pan-Tissue, (B) Skin & Blood, (C) Hannum, (D) PhenoAge, (E) DNAmTL, and (F) GrimAge epigenetic clocks.The linear trendline and 95% CI are plotted as a solid line with shaded area and the identity line (y = x) is plotted as a dashed line.

hours per day standing on feet at workplace during pregnancy Mean mothers' hours per day stooping or bending at workplace during pregnancy Child characteristics
eTable 5.

Comparison of sociodemographic characteristics between included and excluded mother-child pairs. Values represent count (%) or mean (SD).
a Five pregnant participants who were enrolled in the initial CHAMACOS cohort eventually delivered twins.eTable 6.

Adjusted associations between prenatal maternal occupation and child Horvath EAA by child age compared to children whose mothers did not work during pregnancy (ages 7-14 years, N=290)
: Residuals from models regressing Hannum, PhenoAge, and GrimAge EA on chronological age represent epigenetic age acceleration (years).Residuals from models regressing DNAmTL on chronological age represent an age-adjusted estimate of DNAmTL (referred to as DNAmTLadjAge) measured in kilobases.